Abstract
Head and neck cancer, including oral squamous cell carcinoma (OSCC), is the sixth leading malignancy worldwide. OSCC is an aggressive tumor and its prognosis has exhibited little improvement in the last three decades. Comprehensive elucidation of OSCC’s molecular mechanism is imperative for early detection and treatment, improving patient survival. Based on broadly accepted notions, OSCC arises from multiple genetic alterations caused by chronic exposure to carcinogens. In 2011, research revealed 10 key alterations fundamental to cancer cell development: sustaining proliferative signaling, evading growth suppressors, avoiding immune destruction, activating invasion and metastasis, tumor-promoting inflammation, enabling replicative immortality, inducing angiogenesis, genome instability and mutation, resisting cell death, and deregulating energetics. This review describes molecular pathological findings on conventional and novel hallmarks of OSCC prognostic factors. In addition, the review summarizes the functions and roles of several molecules as novel OSCC prognosticators.
Highlights
Head and neck cancer, including oral squamous cell carcinoma (OSCC), is the sixth leading cancer worldwide, with an estimated 300,400 cases and 145,400 OSCC-related deaths occurring in 2012 [1]
The p53 mutation grading system, which classifies low-risk missense mutations, high-risk missense mutations, and other mutations have developed in head and neck cancer containing OSCC, and subgroups of high-risk p53 mutations are associated with decreased sensitivity to cisplatin, distant metastasis, extranodal extension, and poor prognosis [17,18,19]
We investigated the hallmarks of cancer-related molecules to elucidate the molecular mechanism of cancer development, invasion, metastasis, and prognosis
Summary
Head and neck cancer, including oral squamous cell carcinoma (OSCC), is the sixth leading cancer worldwide, with an estimated 300,400 cases and 145,400 OSCC-related deaths occurring in 2012 [1]. OSCC is one of the leading causes of morbidity and mortality in Melanesia, South Central Asia, and Central and Eastern Europe [1]. It arises anywhere in the oral cavity, including the tongue, upper and lower gingiva, oral floor, palate, and buccal mucosa. The p53 mutation grading system, which classifies low-risk missense mutations, high-risk missense mutations, and other mutations have developed in head and neck cancer containing OSCC, and subgroups of high-risk p53 mutations are associated with decreased sensitivity to cisplatin, distant metastasis, extranodal extension, and poor prognosis [17,18,19]. PTEN is inactivated due to gene methylation because PTEN mRNA restoration is observed post-treatment with 5-aza-2 -deoxycytidine (5-Aza-dc), a demethylation reagent, in human OSCC-derived cells [25]
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